This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Objective: To determine fetal, neonatal and adult markers reflecting mechanism of fetal programming of polycystic ovary syndrome (PCOS). This project continues to determine fetal and neonatal consequences of exposing female rhesus monkey fetuses to androgen excess during early gestation. Current results indicate that a hyperglycemic pregnancy induced by the androgen excess given to pregnant rhesus mothers may contribute to altered morphology of pancreatic islets in exposed female infants that may explain functional alterations in insulin-mediated regulation of glucose. This work provides additional direct evidence for fetal programming of metabolic defects in this nonhuman primate model of PCOS. This research used WNPRC Assay Services, Pathology Services and Animal Services. PUBLICATIONS: Abbott DH, Bruns CM, Barnett DK, Dunaif A, Goodfriend TL, Dumesic DA, Tarantal AF. 2010 Experimentally-induced gestational androgen excess disrupts glucoregulation in rhesus monkey dams and their female offspring. Am J Physiol Endocrinol Metab. 299:E741-751. PMID 20682841. Pasquali R, Stener-Victorin E, Yildiz BO, Duleba AJ, Hoeger K, Mason H, Homburg R, Hickey T, Franks S, Tapanainen J, Balen A, Abbott DH, Diamanti-Kandarakis E, Legro RS. PCOS Forum: Research in Polycystic Ovary Syndrome Today and Tomorrow. Clin Endocrinol (Oxf). 2010 Dec 15. doi: 10.1111/j.1365-2265.2010.03956.x. [Epub ahead of print] PMID 21158892.